The expression of activated cellular oncogenes in chemically induced rat tumors and in comparable human neoplasms and the relationship of oncogene expression to progression from the normal to the neoplastic phenotype are being studied using 3T3 transfection and hybridization techniques and monoclonal antibodies directed against the specific oncogene products. The consistent activation of K-ras in rat renal mesenchymal tumors has been shown to occur by a G to A transition mutation in the second position of codon 12, which has been demonstrated in 3T3 transformants and in DNA from primary tumors whether the DNA transformed 3T3 cells or not. Further studies on the neu oncogene in the pathogenesis of schwannomas, in a different strain of rat than was previously used, confirm the consistent presence in an additional 30 such tumors (100% of those tested) of neu activated by a T to A transversion mutation in that segment of the neu locus encoding the putative transmembrane region of the protein encoded by the gene, a growth factor receptor-tyrosine kinase-type molecule. Further studies are in progress to determine whether neu is comparably activated by point mutation in chemically induced schwannomas of other species of rodents and in human tumors including schwannomas.